Clinical Medical College of Yangzhou University, Northern Jiangsu People's Hospital, Yangzhou, 225001, China.
Qilu hospital of Shandong University Dezhou Hospital, Dezhou, 253000, China.
Food Funct. 2022 Oct 3;13(19):9973-9987. doi: 10.1039/d2fo01304e.
Osteoarthritis (OA) is a degenerative joint disease characterized by articular cartilage degeneration, subchondral bone sclerosis, synovial hyperplasia and osteophyte formation as the main pathological manifestations. Age, mechanical stress and inflammation are the main factors that induce joint degeneration in the pathogenesis of OA. Sinensetin (SIN) is a natural flavonoid with anti-inflammatory and antioxidant properties. This study aims to investigate the effect of SIN on OA. We have investigated the anti-inflammatory and chondroprotective effects of SIN on IL-1β-induced human OA chondrocytes and a rat OA model. , human chondrocytes were induced by 5 ng mL IL-1β and treated with different concentrations of SIN. The results suggest that SIN can inhibit IL-1β-induced overproduction of pro-inflammatory mediators in human OA chondrocytes, including COX2, iNOS, TNF-α and IL-6, and also reduce the production of MMP13 and MMP9, thus protecting the degradation of the extracellular matrix. In addition, SIN can inhibit the activation of NF-κB by regulating the expression of SERPINA3. In an experiment, rats were randomly divided into 3 groups, namely the sham operation group, OA model group and SIN group, and were given normal saline or 20 mg kg SIN, respectively. The knee cartilage tissue was removed 6 weeks after surgery for analysis and detection, and our studies have shown that SIN can effectively delay the progression of OA in rats and protect cartilage. In conclusion, our study shows that SIN has good application potential in the treatment of OA.
骨关节炎（OA）是一种退行性关节疾病，其特征为关节软骨退化、软骨下骨硬化、滑膜增生和骨赘形成等主要病理表现。年龄、机械应力和炎症是 OA 发病机制中诱导关节退化的主要因素。橙皮素（SIN）是一种具有抗炎和抗氧化特性的天然类黄酮。本研究旨在探讨 SIN 对 OA 的作用。我们研究了 SIN 对 IL-1β诱导的人 OA 软骨细胞和大鼠 OA 模型的抗炎和软骨保护作用。将人软骨细胞用 5ng/mL IL-1β诱导，并给予不同浓度的 SIN 处理。结果表明，SIN 可抑制 IL-1β诱导的人 OA 软骨细胞中促炎介质的过度产生，包括 COX2、iNOS、TNF-α和 IL-6，同时减少 MMP13 和 MMP9 的产生，从而保护细胞外基质的降解。此外，SIN 可以通过调节 SERPINA3 的表达抑制 NF-κB 的激活。在一项实验中，大鼠被随机分为 3 组，即假手术组、OA 模型组和 SIN 组，分别给予生理盐水或 20mg/kg SIN。手术后 6 周取出膝关节软骨组织进行分析和检测，我们的研究表明，SIN 可有效延缓大鼠 OA 的进展并保护软骨。综上所述，本研究表明 SIN 在 OA 治疗中有很好的应用潜力。
